Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology Med School wk 1 > Cells of the innate immune system > Flashcards

Cells of the innate immune system Flashcards

1
Q

Eosinophils: abundancy, how they stain, granules, rxns, proteins produced

A 
2-5% of white blood cells 
stain red-pink
granules: basic proteins, peroxidases, antimicrobial substances 
involved in EXTRACELLULAR digestion 
inflammatory mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mast cells are

A

tissue fixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

basophils are

A

circulating in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mast/basophils play a role in what awful rxn?

A

anaphalactic rxns?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Basophils stain

A

purple-black

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

basophil granules contain

A

histamine, serotonin, heparin

cytokines, chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Macrophages do what

A

phagocytes and APCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In connective tissue macs are called

A

histocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In the liver macs are called

A

kupfer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

in the alveolar cells they are called

A

alveolar macs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in the CNS they are called

A

microglial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Macrophage

1) produce and release: _____ enzymes
2) produce and release: _____ inflammatory mediators

A

1) lipases/galactosidases
2) cytokines/chemokines
3) ROI
4) NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NK cells

what causes them to destroy?
what are their targets?
What kind of Ag receptor?

A

1) they dont need prior stimulation
2) cancer cells, viral infected cells, transplant cells
3) no specific AG receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What mechanism allows innate immunity to discriminate self/nonself?

A

PAMPs via PRRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PRRs: properties

A

recognize mannose-tails, essential property of surface molecules of bacteria and viruses

germ-line encoded (limited diversity)

nonclonal: identical on all cells

discriminate self/non-self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TLRs do what “ultimately” ?

A

recognize PAMPs and activate inflammation

17
Q

TLRs do what specifically

A

they cause the formation of transcription factors

NF-kB and IRFs.

NF-KB –> acute inflammation
IRFs –> IFN alpha/beta

18
Q

TLRs—> MyD88 adaptor –>

A

IRAK enzymes –> TRAF (goes two ways)

                                  - ---> inactivation of IkB --> NFkB
                                  - ---> induction of MAPK kinases
                                  - ---> pro-inflammatory genes
19
Q

TLR-4

Sequence of events leading to cytokine production

Step 1

A

TLR-4, co-receptor CD14, MD2, and LPS form a complex

CD14 grabs LPS, whose tail interacts on MD2 on TLR-4

20
Q

TLR-4

Sequence of events leading to cytokine production

Step 2

A

TIR domain intracellularly binds to MyD88

MyD88’s death domain interacts with death domain of IRAK4

this causes TRAF-6 to bind IKK

IKK binds IkB, NF-kB

21
Q

TLR-4

Sequence of events leading to cytokine production

Step 3

A

NF-kB activates transcription of genes –> inflammation

22
Q

name all the proteins and their functions in TLR-4 LPS recognition

A

TLR-4

MD2- the bridge between TLR-4-MD2-LPS-CD14

23
Q

LPB

A

LPS binding protein in the blood

24
Q

TIR domain

A

Toll/Interleukin-1 receptor associated kinase 4

domain on the cytoplasmic side of TLR -4

25
Q

IRAK-4

A

interleukin 1 receptor associated kinase 4

26
Q

IKK

A

I kappa B kinase

27
Q

how do PRRs work?

A

receptor recognizes pathogen, phagocytosis occurs, lysosome fuses with phagocyte, kills microbe

interiorly, iNOS or phagocyte oxidase produces NO and ROS

28
Q

Complement:

consists of ? what is their normal state?
what happens during activation?
what do the large fragments forms versus the small fragments?

A

1) serum proteins
2) soluble inactive precursors
3) they are cleaved
4) large form the membrane attack complex
5) small form
a) chemoattractants
b) anaphylatoxins
c) opsonins

29
Q

the large fragment has two sites

A

enzyme site and attachment site

30
Q

what pathways does complement activation have

A

Classical: Ab mediated
Alternative: Ab independent, microbial cell wall activating
lectin: MBL binds microbial carbohydrates in the plasma

CAL

Alt-Mic-MBL

31
Q

what pathway forms MAC?

A

lytic pathway

32
Q

Classical PW overview C3—>

A

C3b, associates with C2a, which associate with C4b linked to a bacterium

C3bC2aC4b = C5 convertase

C5 Con. —> C5 —> C5b and C5a
C5b + C6, 7, 8, 9 = MAC

33
Q

Acute phase proteins

A

circulating proteins, induced rapidly by cytokines after infection

these include MBL and C-reactive protein (CRP)

34
Q

MBL

A

recognizes microbial carbohydrates, activates lectin pathway

35
Q

CRP

A

binds to phosphorylcholine on microbes and coats the microbes for phagocytosis by macrophages

Immunology Med School wk 1 (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions